Prostanoid production in tissues of the reproductive tract is regulated by steroid hormones, but the roles of the individual steroids are not fully understood and seem to vary among species and tissues. In the female, both estrogen and progesterone are involved, apparently in a tissue- and species-specific manner. In the past an association was found with increasing plasma estrogen levels and prostaglandin (PG) production in endometrium and decidua of rats, guinea pigs, rhesus monkeys, and women, and references therein). Estrogen was associated with increased PG production, immunoreactive COX-2 enzyme concentration, and/or COX-2 transcription in endometrial cell cultures from nonpregnant guinea pigs and cows, as well as in rat uterine tissues in vivo. On the other hand, ovarian steroids had no effect on COX-2 gene expression in the mouse uterus in early pregnancy. Progesterone was found to increase COX-2 transcription severalfold and to have no effect on COX-1 mRNA in ovariectomized ewes; administration of estradiol enhanced COX-1 gene expression somewhat.
In endometrium of prepubertal heifers, progesterone pretreatment was necessary for COX-2 transcription and oxytocin (OT)-induced prostaglandin F2a (PGF2a) release in spite of significant reduction of OT receptor concentrations by progesterone. Estrogen treatment had no effect on either parameter, but in combination with progesterone, estradiol caused substantial enhancement of COX-2 mRNA accumulation and PGF2a release.